How to Use the Medicinal effect and Power of DECA: Its Tea Time with OMEGA

[cgar1228]

i never said anything about what you said being bro-ology if you read my post

the way you worded your original post made it sound like you were challenging whether 19-nor testosterone compounds raised prolactin at all

it happens to some, for others it doesnt.

i would love to see bloodwork too btw so hopefully we will be lucky enough to at some point

ps what was your cycle, how much deca did you run etc etc

To an extent I was challenging it but in a way that would encourage someone to post up a blood test or study that shows this to be true. There are thousands of people on this site and not a single one can or has posted up their blood work after their cycle like I did? I guess I got a little feed up with telling people that my prolactin/progesterone was NOT high after asking people what's wrong with my libido and them telling me that this was the case. It's like the go-to answer around here and all I'm asking for is a little proof.

To answer your question Ozzie my cycle was as follows:
400 mg/wk Deca for 10wks
500 mg/wk Test Enth for 12 wks

I actually read a study yesterday about how deca and tren do not increase prolactin at all but actually reduce it. Here is the pertinent part of the study:

Prolactin secretion in the human male is increased by endogenous oestrogens and decreased by exogenous/endogenous androgens.

Gooren LJ, van der Veen EA, van Kessel H, Harmsen-Louman W, Wiegel AR.

There is evidence that prolactin may be involved in testicular steroidogenesis, and we have therefore investigated whether there is feedback regulation of androgens/oestrogens on prolactin secretion in the human male. To assess this we have measured basal and TRH-stimulated prolactin levels in: Six eugonadal men before and after 2 weeks' administration of the aromatase inhibitor delta'-testolactone, which led to a fall in oestradiol levels with unchanged levels of testosterone. In these patients, prolactin levels decreased. Six eugonadal subjects before and after 6 weeks' administration of dihydrotestosterone undecanoate. In these subjects, prolactin levels decreased. Six agonadal subjects, tested after 12 weeks' treatment with dihydrotestosterone undecanoate and compared to: Six agonadal subjects who received no sex steroid treatment. Again, it was found that dihydrotestosterone treatment decreased prolactin levels in patients from Group C. Six eugonadal subjects were also studied before and after 6 weeks' administration of the androgen receptor antagonist, spironolactone, and this treatment increased Prl secretion. It is concluded that in the human male, endogenous oestrogens increase prolactin secretion whilst exogenous/endogenous androgens decrease prolactin secretion


And in male sheep, tren has no effect on prolactin levels:

Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol.

Donaldson IA, Hart IC, Heitzman RJ.

The mode of action of the anabolic steroid trenbolone acetate (19-norandrost-4,9,11-trien-3-one-17-acetate) was studied through the endogenous hormonal response of castrated male sheep to subcutaneous implantation of 140 mg of trenbolone acetate and 20 mg of oestradiol both separately and in combination. Radioimmunoassay of delta-4,9,11-trienic steroids and oestradiol-17 beta in plasma confirmed that simultaneous administration of trenbolone acetate with oestradiol led to a significantly greater persistence of oestradiol-17 beta residues in plasma (P less than 0.05) than with implantation of oestradiol alone. Oestradiol treatment increased concentrations of growth hormone and insulin (P less than 0.05; P less than 0.001 respectively) in plasma samples collected weekly. Trenbolone acetate by itself had no significant effect and the oestrogenic response was blocked on the simultaneous implantation of trenbolone acetate and oestradiol (despite higher plasma levels of oestradiol-17 beta with this treatment). Plasma total thyroxine was markedly depressed to 45 per cent of its basal level by trenbolone acetate, alone or with oestradiol (P less than 0.001) and depressed to 80 per cent of basal by oestradiol treatment alone (P less than 0.001). Plasma prolactin was unaltered by the above treatments.


This study holds true to my blood tests and concludes that deca/tren DO NOT raise prolactin levels. Does anyone have information to show otherwise?

 

[OMEGA]

Cgar
no bro those studies are misleading not even applicable for US on cycles

second study is in sheep bro wtf

First one is with Test levels at a static level(eugonadal)
Second is in sheep lol ( not humans)

The fact is this when your on cycle with Test ( where Test levels are not static) and then you add Deca in, you get the conversion.
Now yes using Ai and Cabergoline could control this but its $$$, so I gave the option of using safe guidelines to avoid sides with spending $$$

 

[cgar1228]

Ozzie/Omega the study I found on male sheep is the ONLY relevant study I have read on this subject. Are you saying that ALL studies that have been done on rats and not humans should be thrown out the window? Why do you think this group of scientists decided to do this particular study on sheep? It's definitely not because they care how sheep react to androgens LOL. It's because this group of scientists, whom I am sure have close correlation on the way the pituitary gland in humans and sheep react with androgens and a more in depth knowledge about this subject than any of us, decided that this would give us a good indication of how WE react to androgens as well. For anyone to throw out this study because it was done on sheep is undermining the knowledge of the scientific community and it's research. So good sir, I believe you have your debate cut out for you.

Again, if this study is not conclusive enough for you along with my blood test then please post a relevant study. Because so far all I've heard arguments with no proof. I am a sponge that is not saturated and not incapable of absorbing new information.

 

[OMEGA]

No Animals only provide a cursory reference point for how things work or "may" work in humans, it is ONLY when the studies are done in humans that you may make a factual beyond a doubt statement (peferably males since females respond different)

case in point; Clen is anticatabolic in rats. So we all assumed years ago it would be in humans. Its NOT for we dont have any of those receptors to respond as rats did.

Let me make another leap.... if xy and Z worked on a cat, am i too assume it would work on a Llamma?
When you make a leap from sex to sex there is a disconnect in results let alone a species jump if you looking for empirical facts on how it will effect us.

 

[OMEGA]

as for as Tests or results.....bro just look at the complaints and sides once you introduce more deca then is needed on a Test Base.

Its not Estro that the culprit , Estro is simply the partner in crime

 

[XMAN.]

I don't have much posts here, but was skimming and read this thread. It's a good read, but I noticed it said "boosts the immune system"

It actually lowers interferon gamma levels (essential in our first line of defense for our immunities), and can actually mask Tuberculosis during testing. A man almost died from TB because the doctor's couldn't figure out what was wrong due to the Deca.

(I don't have enough posts to post the link)

In case readers don't know what interferon is, here is a definition from wiki:

"Interferons (IFNs) are proteins made and released by lymphocytes in response to the presence of pathogens—such as viruses, bacteria, or parasites—or tumor cells. They allow communication between cells to trigger the protective defenses of the immune system that eradicate pathogens or tumors."

also Deca has another scary side effect...

Nandrolone kills the blood vessel lining at a concentration eleven times lower than that at which testosterone kills them. Researchers from the University of L’Aquila in Italy discovered this in laboratory tests on human cells.

Really increases the chance of a heart attack over time
(I don't have enough posts to post a link)


Also it stays in the system so much longer than other steroids and causes more suppression because of this.

I personally would not use deca again

interesting post, does anyone have a clue on this, could it be true? maybe it is dose and length dependent , how it is used for years for hiv patient , muscle wasting disease or any auto-immune disease ?
i wanna know more about these interferons and blood vessels lining , so if u plz can post a real study with references.

 

[tinytim-nor]

Well... animal studies showed no progestagenic activity. And animal studies is all we have on certain steroids.
His bloodwork showed no raised progesterone.

Together it sure beats steroid "profiles" and bro-logic. Most people run many different compounds from various UG-labs and have very little control on what sides are the direct result of which steroids, what is the result of the combinations of steroids or the combination of their various metabolites.

There are too many gurus whose post-counts are seen as an acceptable substitute for real credentials.

Their "wisdom" is parroted across the different boards and before you know it anadrol will make your liver explode (nevermind the 10-year olds who's prescribed anadrol for wasting diseases at high bodybuilding dosages for six months with NO ill effects seen on their livers), tren is a progestin beacuse it BINDS to the progesterone-receptors (nevermind it barely ACTIVATES them), and all 19-nors are alike. Well, they're not, just beacuse part of their chemical structure is the same, they're as different as dianabol and equipose. Which is the same steroid. Except it isn't, regardless of structure.

Use pure compounds.
PURE.
In isolation.
Get bloodwork.
Then combine two.
Get bloodwork again.

Now one can begin to form an opinion based on what MAY be fact.

Or be a parrot. Nevermind pubmed, animal studies or facts.

 

[cgar1228]

No Animals only provide a cursory reference point for how things work or "may" work in humans, it is ONLY when the studies are done in humans that you may make a factual beyond a doubt statement (peferably males since females respond different)

case in point; Clen is anticatabolic in rats. So we all assumed years ago it would be in humans. Its NOT for we dont have any of those receptors to respond as rats did.

Let me make an even larger leap.... if xy and Z worked on a cat, am i too assume it would work on a Llamma?
When you make a leap from sex to sex there is a disconnect in results let alone a species jump if you looking for empirical facts on how it will effect us.

A sheep's pituitary gland more closely represents the size and function of the human pituitary than any other animal, even in relation to the female pituitary. I think it's safe to say that me using this study to represent my theory is a whole lot better than you trying to argue your point with NO study to back your claims.

We react the same way as animals with a pituitary to injecting gonadotropic hormones which makes the pituitary produce LH and send it to the leydig cells. It doesn't sound like the SCIENTIST that decided to use MALE sheep to simulate what would happen in humans were off base at all. All I'm saying is, if you want to make a point then use research to back yourself.

 

[OMEGA]

oh my gosh cgar lol Im sorry but you cant compare them. believe if you want or not.

none the less thanks for sharing

 

[cgar1228]

again WE ARE NOT SHEEP!!!!

how can you say just because it doesnt have that effect on sheep, that it wont have an effect on us?

yes it might be the most similar to a human for the test, but at the end of the day its a sheep! if i started eating grass all day would i grow a nice wooley coat?? i doubt it (although that would be funny!)

and also how can you explain the fact that so many steroid users have HAD to use drugs to lower prolactin in order to fix deca/tren side effects?

if these side effects did not exist then the treatment would be useless and have zero effect.

the fact that the use of cabergoline, whos medical purpose is to lower prolactin, solves the problems commonly caused by progestenic steroid use in humans , is far more conclusive than a study done on sheep IMO

So youre saying were NOT sheep.... interesting.

You would look stellar with a wooley coat. I wouldn't necessarily say that you would grow one if you at grass all day, but you 'might' get some action if you slipped a roofie in it's water bowl and brought a pair of velcro gloves. LOLOLOL

On the argument of sheep's pituitary vs humans, would it be fair to say that since not ALL humans are subject to prolactin issues while taking deca/tren, do you think it's possible that the sample 'lab sheep' tested didn't accurately represent the sheep population and there are still sheep out there vulnerable to the dreaded 'Deca Dick'?